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血管性癡呆小鼠海馬線粒體復(fù)合體活性變化

發(fā)布時(shí)間:2018-05-03 02:24

  本文選題:血管性癡呆 + 記憶; 參考:《中國(guó)醫(yī)院藥學(xué)雜志》2015年16期


【摘要】:目的:探討血管性癡呆(VD)小鼠海馬線粒體復(fù)合體活性變化。方法:抽取并回輸約40%總血量加雙側(cè)頸總動(dòng)脈夾閉20 min建立VD模型。病理學(xué)研究檢測(cè)神經(jīng)元損傷;分光光度計(jì)法檢測(cè)丙二醛(MDA)含量、錳超氧化物歧化酶(Mn-SOD)活性和線粒體復(fù)合體活性;Western-blot檢測(cè)Mn-SOD蛋白表達(dá);Morris水迷宮評(píng)估學(xué)習(xí)記憶能力。結(jié)果:與假手術(shù)組相比,模型組學(xué)習(xí)記憶能力顯著降低(P0.05),MDA含量顯著升高(P0.05),Mn-SOD活性和蛋白表達(dá)顯著降低(P0.05);與假手術(shù)組相比,術(shù)后5 d模型組線粒體復(fù)合體Ⅰ、Ⅱ、Ⅲ、Ⅳ活性顯著降低(P0.05),術(shù)后15,30 d和60 d模型組線粒體復(fù)合體Ⅰ、Ⅱ活性無(wú)顯著變化(P0.05),復(fù)合體Ⅲ、Ⅳ活性顯著降低(P0.05);病理學(xué)檢測(cè)顯示模型組海馬出現(xiàn)進(jìn)行性神經(jīng)元損傷。結(jié)論:線粒體復(fù)合體III、IV活性異?赡苁荲D的發(fā)病機(jī)制之一。
[Abstract]:Objective: to investigate the changes of mitochondrial complex activity in hippocampus of vascular dementia (VD) mice. Methods: the VD model was established by extracting and regurgitating 40% total blood volume and bilateral common carotid artery occlusion for 20 min. The neuronal damage was detected by pathology, the content of malondialdehyde (MDA), the activity of manganese superoxide dismutase (Mn-SOD) and the activity of mitochondrial complex (Mn-SOD) were detected by spectrophotometer, and the expression of Mn-SOD protein by Morris water maze was detected by Western-blot to evaluate the ability of learning and memory. Results: compared with the sham-operated group, the learning and memory ability of the model group was significantly lower than that of the sham-operated group, and the MDA content of the model group was significantly higher than that of the sham-operated group, and the activity and protein expression of P0.05Mn-SOD were significantly lower than that of the sham-operated group, and the mitochondrial complex 鈪,

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